Journal
MOLECULAR AND CELLULAR BIOLOGY
Volume 22, Issue 16, Pages 6014-6022Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.22.16.6014-6022.2002
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Funding
- NCI NIH HHS [P30 CA016087, P30CA16087] Funding Source: Medline
- NIAID NIH HHS [AI29963, R01 AI029963] Funding Source: Medline
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We recently discovered that heat shock causes nucleolin to relocalize from the nucleolus to the nucleoplasm, whereupon it binds replication protein A and inhibits DNA replication initiation. We report that nucleolin mobilization also occurs following exposure to ionizing radiation (IR) and treatment with camptothecin. Mobilization was selective in that another nucleolar marker, upstream binding factor, did not relocalize in response to IR. Nucleolin relocalization was dependent on p53 and stress, the latter initially stimulating nucleolin-p53 complex formation. Nucleolin relocalization and complex formation in vivo were independent of p53 transactivation but required the p53 C-terminal regulatory domain. Nucleolin and p53 also interact directly in vitro, with a similar requirement for p53 domains. These data indicate a novel p53-dependent mechanism in which cell stress mobilizes nucleolin for transient replication inhibition and DNA repair.
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